Journal of Hazardous Materials

Metal(loid) salts have been used to treat infectious diseases due to their exceptional biocidal properties at low concentrations. However, the mechanism of their toxicity has yet to be fully elucidated. The production of reactive oxygen species (ROS) has been linked to the toxicity of soft metal(loid)s such as Ag(I), Au(III), As(III), Cd(II), Hg(II), and Te(IV). Nevertheless, few reports have described the direct, or ROS-independent, effects of some of these soft-metal(loid)s on bacteria, including the dismantling of iron-sulphur clusters [4Fe-4S] and the accumulation of porphyrin IX. Here, we used genome-wide genetic, proteomic, and biochemical approaches under anaerobic conditions to evaluate the direct mechanisms of toxicity of these metal(loid)s in Escherichia coli. We found that certain soft-metal(loid)s promote protein aggregation in a ROS-independent manner. This aggregation occurs during translation in the presence of Ag(I), Au(III), Hg(II), or Te(IV) and post-translationally in cells exposed to Cd(II) or As(III). We determined that aggregated proteins were involved in several essential biological processes that could lead to cell death. For instance, several enzymes involved in amino acid biosynthesis were aggregated after soft-metal(loid) exposure, disrupting intracellular amino acid concentration. We also propose a possible mechanism to explain how soft-metal(loid)s act as proteotoxic agents.

Microbial arsenic methylation is established as a detoxification process under aerobic conditions (converting arsenite to monomethylated arsenate) but proposed to be a microbial warfare strategy under anoxic conditions due to the toxicity of its main product monomethylarsonous acid (MMAs(III)). Here, we leveraged a paddy soil-derived anaerobic arsenic methylator, Paraclostridium bifermentans strain EML, to gain insights into this process. Strain EML was inoculated into a series of media involving systematic dilutions of Reinforced Clostridial Broth (RCB) with 25 M arsenite to assess the impact of growth substrate concentration on arsenic methylation. Growth curves evidenced the sensitivity of strain EML to arsenite, and As speciation analysis revealed the production of MMAs(III). Concentrations of MMAs(III) and arsenic methylation gene (arsM) transcription were found to be positively correlated with the RCB dilution, suggesting that substrate limitation enhances arsM gene expression and associated anaerobic arsenic methylation. We propose that growth substrate competition between microorganisms may also lead to an increase in anaerobic As methylation. This hypothesis was further evaluated in an anaerobic co-couture mode of strain EML with either wild-type Escherichia coli K-12 MG1655 (WT) or E. coli expressing the MMAs(III)-resistance gene (arsP), (ArsP E. coli). We found increased MMAs(III) production in the presence of E. coli than its absence and growth inhibition of WT E. coli to a greater extent than ArsP E. coli, presumably due to MMAs(III) produced by strain EML. Taken together, our findings point to an ecological role for anaerobic arsenic methylation, highlighting the role of microbe-microbe competition/interaction in this process. IMPORTANCEAnaerobic arsenic methylation is enhanced in rice paddy soils under flooding conditions than that under drying conditions, leading to increased methylated arsenic accumulation in rice grains. Unlike the known detoxification role for aerobic arsenic methylation, the ecological role of anaerobic arsenic methylation remains elusive and is proposed to be an antibiotic-producing process involving in microbial warfare. In this study, we interrogated a rice paddy soil-derived anaerobic arsenic-methylating bacterium (Paraclostridium bifermentans strain EML) to investigate the effect of growth substrate limitation on arsenic methylation by strain EML in the context of the microbial warfare hypothesis. We provide direct evidence for the role of growth substrate competition in anaerobic arsenic methylation by strain EML. Furthermore, we evidence a feedback loop, by which a bacterium resistant to MMAs(III) enhances its production, presumably through enhanced arsM expression resulting from substrate limitation. Our work uncovers complex interactions between an anaerobic arsenic methylator and potential competitors.

Extensive mineral weathering and formation of large amounts of Fe-rich secondary mineral gels have been identified as precursors critical to forming massive hardpan caps in the surface layers of sulfidic tailings. However, how to initiate and accelerate these precursor processes remains to be established before developing this hardpan-based novel method to rehabilitate sulfidic tailings landscapes. In a 5-month microcosm experiment, the present study has demonstrated the concept of bio-engineering sulfidic tailings by inoculating Fe/S-oxidizing bacterial consortium to accelerate the weathering of sulfides and other Si-rich minerals for mineral gels formation. Synchrotron-based X-ray absorption fine structure spectroscopy (XAFS) demonstrated that the weathering of pyrite and biotite-like minerals was rapidly accelerated by the presence of Fe/S-oxidizing bacterial consortium. The microbial process and associated mineral transformation led to the formation of critical precursor mineral gels, i.e., jarosite-like minerals, as indicators of the onset of hardpan formation. In the meantime, the labile Zn liberated in the weathering was encapsulated in the jarosite-like minerals as revealed by X-ray fluorescence microscopy (XFM). This concept-proven bio-engineering process is ready to be scaled up in further studies under field conditions to develop an alternative hardpan-based method to cover and rehabilitate sulfidic tailing landscapes. TOC Art O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=145 SRC="FIGDIR/small/285858v1_ufig1.gif" ALT="Figure 1"> View larger version (83K): org.highwire.dtl.DTLVardef@fc0292org.highwire.dtl.DTLVardef@10ce8c7org.highwire.dtl.DTLVardef@868a63org.highwire.dtl.DTLVardef@e77d57_HPS_FORMAT_FIGEXP M_FIG C_FIG

Mesoporous nanoparticles (NPs) are an interesting drug delivery system that has generated considerable attention in the biomedical sector. Despite recent attempts to conduct safety assessments using traditional methods based on phenotypic data, our understanding of the underlying molecular processes produced by mesoporous NPs is still in its infancy. In the present study, RNA sequencing was used to assess the biological perturbations and the pathways induced in response to early exposure of two different mesoporous NPs; mesoporous silica NPs (MSN) and mesoporous carbon NPs (MCN) in human liver hepatocellular carcinoma cells. In order to better understand the risks associated with NPs, it is required to consider the initial low-dose exposure effects that mimic the real exposure scenario. No overt toxicity was detected in the MTT assay when performed at 6 hours at low concentrations (MCN 25 g/ml and MSN 15 g/ml) of NPs; thus, we have selected this dose for RNA sequencing analysis. Our transcriptomics analysis showed significant differences in the expression of many genes after exposure to both NPs. Surprisingly, both NPs frequently deregulated 52.9 percent of upregulated and 42 percent of downregulated genes. Gene ontology categories, in particular, revealed comparable perturbations of biological reactions in the cellular system. HepG2 cells reacted to mesoporous NPs by allowing alterations in genes involved in cytoskeleton reorganisation (ATAT1, DMTN, PTK2 and PFN2). Exposure to mesoporous NPs increased transcripts expressing ubiquitin ligase (RNF187, ARIH2, VHL, and RAB40C), transferase (FBXO3 and WDSUB1), conjugating (UBE2J2), and also proteasomal subunits (PSMD2, PSMD13) enzymes, indicating that protein turnover rates are altered in response to environmental damage. In addition, DNA damage and DNA damage checkpoint genes were upregulated, indicating that NPs induced stress in the cells. These finding showed low dosage acute exposure have comparable responses between mesoporous NPs. These results may add further knowledge in conceptualization of Safer-by-Design strategy of NPs in biomedical field.

Anthropogenic activities are driving an increasing flux of rare earth elements (REE) into environmental compartments, raising concerns about their biological impact, particularly on microorganisms that sustain ecosystem functioning. Here, we provide a systematic assessment of the toxicity of all 16 REE toward Pseudomonas putida KT2440, a soil bacterium that can use these metals as enzyme cofactors. Dose-response growth inhibition assays revealed high sensitivity to light REE. Toxicity correlated strongly with ionic radius, with IC50 values ranging from 0.3 {micro}M for lanthanum to 10 {micro}M for scandium. Serial propagation of P. putida under gradually increasing REE stress yielded resistant populations, from which two stably resistant strains were isolated. Genome resequencing showed that both strains carried a single mutation in uxpB, encoding an alkaline phosphatase. Gene deletion and overexpression experiments, together with phosphatase activity measurements, confirmed the involvement of uxpB in REE resistance. Our findings reveal a previously unrecognized mechanism of tolerance to REE, suggesting that mutations enhancing phosphatase activity promote phosphate release from organic phosphorus compounds and REE immobilization, thereby mitigating toxicity.

Nanoparticles (NPs) are important in a variety of sectors, including disease diagnostics, medicine, nutrition, and many other industries. The risk of human exposure demands an early evaluation of both the basic dynamics of NPs interaction with biological systems and their potential consequences. Deciphering these occurrences will provide critical information regarding the health hazards and safety advantages associated with next-generation nanoformulations in clinical practice. We examined the HepG2 cell line in a systematic manner to determine the cellular response to single-walled carbon nanotubes (SWCNTs) and zinc oxide (ZnO) NPs. With the use of high-throughput transcriptomic methods, we found that both NPs induce comparable dysregulation of the endocytic and proteasomal complex genes in liver hepatocellular carcinoma cells, at levels (> 80 percent cell viability) that do not cause over-toxicity at early incubation period (6 h). SWCNT and ZnO NPs were shown to enter cells through clathrin-mediated pathways, affecting cytoskeleton gene expression, DNA damage and repair, protein ubiquitination, and cell transcriptional machinery. Our findings indicate that early response strategies activate stress-related mechanisms. Finally, this method for studying nanomaterial-cell interactions demonstrates how changes in the transcriptome profile may predict downstream consequences even at doses that do not cause acute toxicity.

Airborne nanoplastics constitute an emerging class of environmental contaminants, but their mitoepigenetic effects on human immune cells have not been systematically investigated. Ex vivo human lymphocytes were used to investigate integrated mitochondrial, epigenetic, and inflammatory responses induced by polystyrene (PS), polypropylene (PP), and polyvinyl chloride (PVC) nanoplastics. Fluorescence microscopy at multiple exposure time points and flow cytometry confirmed efficient cellular internalization and progressive intracellular accumulation of nanoplastics. Exposure elicited coordinated transcriptional remodeling of genes regulating mitochondrial dynamics (DRP1, MFN1), mitochondrial DNA encoded oxidative phosphorylation components (MT-ATP6, MT-COX1, MT-ND6), DNA repair (OGG1, APE1), DNA methylation machinery (DNMT1, DNMT3a, DNMT3b), and mitochondrial-associated miRNAs (miR-21, miR-34a, miR-155). Functional analyses revealed polymer and time-dependent disruption of mitochondrial membrane potential and respiratory chain activities, with Complex I identified as the primary site of vulnerability. Correlation analysis showed strong positive associations among DRP1, OMA1, DELE1, and ND6 (r > 0.9, R{superscript 2} > 0.8, p < 0.001), reflecting coordinated mitochondrial stress and epigenetic signaling, while negative correlations between DRP1 and MFN1 (r = -0.54, R{superscript 2} = 0.29, p < 0.01) and between APE and ND6 (r {approx} -0.42, R{superscript 2} {approx} 0.18, p < 0.05) highlight antagonistic regulation and impaired mitochondrial network stability linked to Complex I dysfunction. In silico docking of oxidized nanoplastic oligomers identified high-affinity interactions at the Complex I Fe-S cluster and cofactor-binding sites, suggesting direct interference with electron transfer. A random forest-based model accurately predicted MT-ND6 expression from Complex I activity (R{superscript 2} > 0.85), establishing a data-driven Complex I-ND6 axis. Collectively, these findings demonstrate that airborne nanoplastics induce integrated mitoepigenetic and immunometabolic dysregulation, underpinned by coordinated and antagonistic regulatory interactions in lymphocytes.

Arsenic (As) poses a major threat to rice productivity and food safety due to its high bioaccumulation potential and subsequent entry into the human food chain. In rice, As impairs seed germination, disrupts morpho-anatomical development, and induces oxidative stress. This study evaluates seed priming with an aqueous extract of the agricultural weed Amaranthus viridis (AvE) as a sustainable strategy to alleviate As-induced phytotoxicity. AvE priming significantly improved germination (71-75%) and morpho-physiological performance under As stress. It reduced oxidative stress markers, including H2O2 (21-38%), malondialdehyde (13-26%), and proline (18.9-44.7%), while increasing antioxidant metabolites, polyphenols and glutathione by up to 2.34-fold and 41%, respectively. Microscopy confirmed restoration of cellular integrity and anatomical organisation in primed seedlings. ICP-OES analysis showed that AvE priming reduced root As uptake by up to 39%, root-to-shoot translocation by up to 58%, and grain As accumulation by up to 95% compared with unprimed plants. qRT-PCR revealed modulation of genes involved in As homeostasis, indicating coordinated physiological and transcriptional responses. Importantly, improved agronomic performance further demonstrated the translational potential of this approach. This study provides the first evidence that A. viridis extract is a cost-effective, sustainable biostimulant for producing low-As rice in contaminated regions.

Tellurium (Te) is a rare element in the chalcogen group, and its biogeochemical cycle has been investigated for decades. As the most soluble Te species, tellurite (Te(IV)) possess the highest toxicity to the organisms. Chemical or biological Te(IV) reduction to elemental tellurium (Te0) is generally considered as an effective detoxification route for Te(IV)-containing wastewater. Here, we reported a previously overlooked Te0 oxidation process mediated by manganese-oxidizing bacterium Bacillus sp. FF-1. This strain has both Mn(II)-oxidizing and Te(IV)-reducing activities, which could produce manganese oxides (BioMnOx) and Te0 (BioTe0) when incubating with Mn(II) and Te(IV), respectively. Te(IV) can co-precipitated with Mn(II) to form highly stable Te(IV)-Mn(II) compounds with low bioavailability. While when 5 mM Mn(II) was added after incubating 0.1 mM or 1 mM Te(IV) with strain FF-1 for 16 hours, the BioTe0 were certainly re-oxidized to Te(IV) by BioMnOx according to the results of X-ray photoelectron spectra (XPS) and Transmission electron microscope (TEM). The chemogenic and exogenous biogenic Te0 can also be oxidized by the BioMnOx, although with different rates. This study highlights a new transformation process of tellurium species mediated by manganese-oxidizing bacteria, revealing that the environmental fate and ecological risks of Te0 needed to be re-evaluated. ImportanceBiogeochemical cycle of Te mediated by bacteria mainly focus on the Tellurite reduction and methylation. In this study, the indirect tellurium (Te0) oxidation driven by manganese-oxidizing bacterium is firstly confirmed. As Te0 usually considered as a stable and safe products during Te(IV)-containing wastewater treatment, we suppose the ecological risks of Te0 needed to be re-evaluated due to the possible oxidation by manganese-oxidizing bacterium and its generated manganese oxides.

Inorganic arsenic is a widespread environmental contaminant and known human carcinogen, yet the mechanisms by which nutritional status modulates arsenic toxicity remain poorly understood. Here, we investigated the main and interactive effects of environmentally relevant concentrations of arsenic, low food quantity, and low dietary phosphorus supply on genome-wide gene expression in aquatic grazer Daphnia pulex. Differential gene expression analysis identified a total of 1,213 differently expressed genes with interactions of arsenic x nutrient stressors accounting for approximately 70% of the transcriptomic response. Low phosphorus emerged as a dominant main effect stressor and it also had a profound impact on transcription as a co-stressor. The low phosphorus x arsenic interaction exhibited the greatest transcriptional impact (435 DE genes), revealing that phosphorus limitation rather than food quantity influences arsenic toxicity at the gene expression level. Gene ontology and Pathway Activation Analysis revealed that main effects elicited simple yet distinct functional responses, whereas arsenic x nutrient interactions induced complex pathway-level disruptions including cell signaling, detoxification metabolism, DNA repair mechanisms, and energy homeostasis. Further assessment of gene expression revealed that all arsenic x nutrient interactions are antagonistic supporting previous literature that found arsenic behaves antagonistically as a co-stressor. Our results provide mechanistic insight into how nutritional status modulates arsenic toxicity and highlights the importance of considering arsenic x nutrient co-stressor interactions.

Copper is an essential redox-active micronutrient, but agricultural soils are increasingly contaminated by copper from mining, industrial discharge, and intensive agrochemical use, pushing concentrations beyond levels plants can tolerate. Excess copper triggers Fenton-like reactive oxygen species (ROS) generation, mitochondrial dysfunction, and impaired growth. Existing mitigation strategies, such as soil amendments, phytoremediation, antioxidants, and different chelators, have been explored to reduce copper toxicity, but their effectiveness can be limited by immobilization, poor specificity, and environmental persistence. The present work introduces a nanoparticle-based strategy for the direct sequestration of excess copper coupled with protection against the oxidative damage caused by copper stress. Here, we report MPA-iron oxide nanoparticles (MIONPs), sequentially functionalized with chitosan, glutathione, and 3-mercaptopropionic acid, designed to simultaneously scavenge ROS, restore redox homeostasis, and chelate copper via surface thiol groups. MIONPs showed a significant increase in copper binding capacity over bare iron oxide nanoparticles (BIONPs) and, in copper-stressed Solanum lycopersicum seedlings, significantly improved germination and root/shoot growth, reduced intracellular ROS, restored mitochondrial membrane potential, and preserved nuclear integrity. This integrated design establishes MIONPs as a promising, dual-function nanoplatform for sustainable copper stress management in agriculture.

The discovery of cisplatin and its anti-tumor activities but also its side-effects led to the development of new cytotoxic metal complexes. Metal-based compounds and especially gold N-heterocyclic carbene complexes have shown their antitumoral activities and present a great interest of use in medicine. These metallodrugs have been shown to target nuclear DNA, but also other organelles such as mitochondria. The mechanisms of action have been studied and would involve the triggering of cell death, in particular by apoptosis, highlighting mitochondrial dysfunctions. The organometallic compound used in this study has been characterized by its IC50 and GI50 in two prostatic cancer cell lines (LNCaP and PC3). Its capacity to enter the cells and particularly mitochondria was also analyzed. Furthermore, its effects on several parameters (proliferation, cell death, cell cycle) have been determined in vitro. The compound displayed a cytotoxic effect (IC50 < 5{micro}M) confirmed by the MTT assays and cell death analysis by flow cytometry. It also displayed a cytostatic effect confirmed by the determination of the GI50, and induced a brief cell cycle arrest, depending on the cell line and the metallocarbene concentration. Furthermore, the incubation with the gold N-heterocyclic carbene led to mitochondrial membrane potential changes and decreased the accumulation of the mitochondrial protein Rieske. All our results show a global cytotoxic and cytostatic effects of the gold N-heterocyclic carbene that can involve mitochondria.

This study presents the first exploratory assessment of antibiotic resistance genes (ARGs) and antibiotic residues in agricultural environments on Reunion Island, a French tropical territory in the south-western Indian Ocean. Sixteen samples from diverse matrices (manure, soil, water, and vegetables) across different agroecosystems were analyzed using high-throughput qPCR targeting 332 ARGs and chemical methods targeting 58 antibiotic compounds and trace elements. ARGs were widely detected across all matrices, with highest abundance observed in amended soils and manure. Surprisingly, ARG profiles, in terms of both abundance and average number, were comparable between unamended soils and natural soils. Antibiotic residues were found in only five manure and soil samples, with no clear correlation between the presence of these residues, trace elements and ARG abundance. Organic amendments significantly increased ARG levels in soils and non-metric multidimensional scaling revealed that ARG profiles clustered primarily by matrix type rather than by location. High-risk ARGs were widely prevalent, with 86% detected and 23% ubiquitous across all samples, and their occurrence in water and raw vegetables suggests potential human exposure through the food chain. This study highlights the influence of agricultural practices on environmental antimicrobial resistance in tropical island contexts and supports the need for expanded One Health surveillance integrating the environmental, animal and human compartments. SynopsisThis study shows that agricultural practices can shape the environmental spread of antibiotic resistance in tropical island ecosystems, highlighting potential risks for ecosystems, food safety, and human health. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=73 SRC="FIGDIR/small/702181v1_ufig1.gif" ALT="Figure 1"> View larger version (31K): org.highwire.dtl.DTLVardef@1d07b87org.highwire.dtl.DTLVardef@5e1150org.highwire.dtl.DTLVardef@1c2afe4org.highwire.dtl.DTLVardef@a9be55_HPS_FORMAT_FIGEXP M_FIG C_FIG

Several studies have been conducted on human exposure to ultrafine particulate matter (UFPM), Black carbon (BC), and polystyrene nanoplastics (PS-NPs). However, it remains unclear whether different chemical types of environmental nanoparticles induce a similar mitochondrial stress response or a unique particle-specific response. In the present study, we examined the molecular mechanisms underlying nanoparticle-induced mitochondrial stress response and immunotoxicity using human peripheral blood mononuclear cells exposed to UFPM, BC, and PS-NPs under similar experimental conditions. Oxidative stress, mitochondrial adaptation, respiratory chain integrity, mitochondrial integrated stress response, inflammatory signaling, and systems-level interactions between molecules were analyzed through the evaluation of the expression of NRF2, HIF-1, PGC-1, TFAM, OMA1, DELE1, mitochondrial ND1, Complex I-V, NF-{kappa}B, TNF-, and NLRP3 and the use of principal component analysis, hierarchical clustering, and correlation networks. All three nanoparticles caused oxidative stress and mitochondrial dysfunction with different kinetics and mechanisms. UFPM mostly induced an acute antioxidant response and mitochondrial adaptation; BC led to chronic mitochondrial dysfunction, chronic activation of the OMA1-DELE1-mediated mitochondrial ISR pathway, and inflammation; while PS-NPs induced low but chronic mitochondrial adaptation along with mitochondrial biogenesis and stress responses. Our systems-level analysis showed that oxidative stress, mitochondrial adaptation, mitochondrial ISR, and inflammation represent a highly connected molecular network regardless of the physicochemical nature of the nanoparticles, with the OMA1- DELE1 axis being a key regulatory node connecting mitochondrial stress response and inflammation. Overall, we have found that mitochondrial stress response is a common mechanism underlying the toxicity of chemically different nanoparticles and have also revealed particle-specific stress-response dynamics responsible for the degree and persistence of cellular damage. The current work presents novel insights into the molecular mechanisms of nanoparticle-induced immunotoxicity and suggests OMA1, DELE1, NRF2, PGC-1, TFAM, ND1, and Complex I-V as potential biomarkers.

Application of carbonaceous nanomaterials (CNMs) to the soil-plant system can affect plant physiology, with positive results ranging from enhanced seed germination and root system development to improved stress tolerance. The underlying mechanisms are not fully understood. Plant rhizosphere microbiomes at the soil-root interface are strongly influenced by the host plant and play a key role in the plant hosts development and health. Yet few studies have characterized changes in plant rhizosphere microbiomes following applications of CNMs to the soil-plant system. Here we investigated the effects of multi-walled carbon nanotube (CNT) and graphene on microbial communities in the ectorhizosphere of tomato plants versus surrounding bulk soil. Pot experiments were conducted where tomato plants were exposed to CNT or graphene at 200 mg/kg soil for four weeks. Ectorhizosphere and bulk soils were then collected and analyzed for physicochemical properties and microbiome structure and function. While graphene had a limited impact on the tomato rhizosphere microbiome, CNT significantly increased microbial alpha diversity, induced greater divergence of beta diversity, enhanced microbial interactions, and potentially impacted community functions such as aromatic compound degradation, antioxidant synthesis, and redox cofactor biosynthesis. Furthermore, CNT induced stronger and/or unique microbiome alterations in the tomato rhizosphere compared to bulk soil. Our findings reveal the differential modulating effects of two widely-used CNMs on plant rhizosphere microbiomes and highlight an imminent need to understand complex plant root-microbe interplays in the CNM-impacted rhizosphere. These results have implication for realizing the full potential of phytoapplication of CNMs toward improved and sustainable plant production.

Bacteria innately monitor their environment by dynamically regulating gene expression to respond to fluctuating conditions. Through synthetic biology, we can harness this natural capability to design cell-based sensors. Bacillus megaterium, a soil bacterium, stands out due to its remarkable heavy metal tolerance and sporulation ability, making it an ideal candidate for heavy metal detection with low transportation costs. However, challenges persist: the synthetic biology toolkit for this strain is underdeveloped and conventional whole-cell sensors necessitate specialized laboratory equipment to read the output. In our study, we genetically modified B. megaterium for arsenic detection, establishing a detection threshold below the EPA recommendation of 10 ppb for drinking water in both vegetative cell form and spore form. Additionally, we integrated both engineered B. megaterium living cells and spores with CMOS chip for field-deployable arsenic detection. We show that the limit of detection of our integrated sensor is applicable in soil and air arsenic contamination testing. As a proof of concept, this work paves the way for deploying our sensor in resource-limited settings, ensuring real-time arsenic detection in challenging environments. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=108 SRC="FIGDIR/small/604150v1_ufig1.gif" ALT="Figure 1"> View larger version (29K): org.highwire.dtl.DTLVardef@1940e83org.highwire.dtl.DTLVardef@144da0aorg.highwire.dtl.DTLVardef@146e906org.highwire.dtl.DTLVardef@6cb8c1_HPS_FORMAT_FIGEXP M_FIG C_FIG

Various environmental aged plastic wastes were collected in the environment and crushed to the nanometric scale to get a mix of nanoplastics (NPs) of different natures - mostly polyolefins (PE, PP), polyesters (PET) and polyvinylics (PS and PVC) - and undefined shapes (noted NP-L, mean hydrodynamic diameter at 285 nm). We aimed to test the toxicity of NPs of environmentally relevance on freshwater bivalves and compare results to commonly used styrenic NP-PS (206 nm). Corbicula fluminea were exposed to four different conditions with NPs (0.008 to 10 g/L), for 21 days and kept under depuration conditions for 21 additional days: 1) waterborne exposure to NP-L, 2) diet borne exposure to NP-L, 3) synergic waterborne exposure to NP-L and AlCl3 salt (1 mg/L), 4) waterborne exposure to NP-PS. Enzyme activities, gene expressions and behavioural tests were assessed. Trophic and synergic exposures with Al triggered more gene modulations than direct exposure to NP-L (namely on 12s, atg12, gal, segpx, p53 and ache). NP-PS were also more harmful than NP-L, but only at high concentrations (10 g/L). The effects of each treatment lasted until 7 days of depuration and no more gene inductions were observed after 21 days in clean water. Very few effects were shown on phenol-oxidase (PO), and glutathione S-transferase (GST). However, the inhibition of acetylcholinesterase (AchE) was concomitant with an increase of the filtration activity of bivalves exposed to NP-L (trophic route) and NP-PS, suggesting neurotoxic effects. By disturbing the ventilatory activity, NPs could have direct effects on xenobiotic accumulation and excretion capacities. The results point out how the structure, aging, exposure routes and additional xenobiotics can interact with adverse outcomes of NPs in bivalves. These findings underline the importance to consider naturally aged environmental NPs in ecotoxicological studies rather than synthetic latexes, i.e. crosslinked nanospheres prepared from virgin polymers. This manuscript presents the first data of toxicity on freshwater organisms exposed to nanoplastics coming from natural sources. Whereas the majority of papers are dealing with non-environmentally representative plastics (mainly commercially-available polystyrene latexes) to evaluate nanoplastic effects on organisms, this study develops methods to prepare model nanoplastics from plastic wastes collected in rivers, and to assess their real adverse effects on aquatic organisms. Our results show significant differences between the inflammatory effects triggered by nanoplastics coming from natural sources and polystyrene nanobeads. This work suggests that the data published so far in the literature may underestimate the toxicity of nanoplastics spread into the environment on the aquatic organisms at the bottom of the food chain, which might consequently impart halieutic resources on the long term.

Environmentally-friendly and low emission extraction methods are needed to meet worldwide rare earth element (REE) demand. Within a greenhouse setting, we assessed the REE hyperaccumulation ability of four plant species (e.g., Phalaris arundinacea, Solanum nigrum, Phytolacca americana, and Brassica juncea) and the impact of amending REE-rich soil with biochar or fertilizer and watering with citric acid solution. Harvested samples were pyrolyzed, and the resulting bio-ores were acid-digested and underwent elemental analysis to determine REE content. Amending soil with fertilizer and biochar increased bio-ore production, while plant species explained most variation in bioaccumulation factor. Phalaris arundinacea achieved the highest average REE concentration of 27,940 ppm for targeted REEs (i.e., cerium, lanthanum, neodymium, praseodymium, and yttrium) and 37,844 ppm for total REEs. We successfully extracted REE-rich bio-ore from plant biomass and determined that soil amendment and plant species will be critical parameters in design and implementation of Idaho-based REE phytomining operations. Graphical Abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=115 SRC="FIGDIR/small/606409v1_ufig1.gif" ALT="Figure 1"> View larger version (48K): org.highwire.dtl.DTLVardef@f616a6org.highwire.dtl.DTLVardef@490d9borg.highwire.dtl.DTLVardef@1c6a72org.highwire.dtl.DTLVardef@1908340_HPS_FORMAT_FIGEXP M_FIG C_FIG

Toxicants in the environment can significantly impact physiology. Environmental chemical exposures during early developmental stages disturb normal embryonic development and programming, and dramatically impact long-term health as individuals age. Female and male animals show distinct phenotypes when responding to a given chemical exposure. Here, through the TaRGET II (Toxicant Exposures and Responses by Genomic and Epigenomic Regulators of Transcription) consortium, we systematically explored sex-specific transcriptomic and epigenomic alterations in response to various toxicants, including arsenic (As), lead (Pb), tributyltin (TBT), bisphenol A (BPA), di(2-ethylhexyl) phthalate (DEHP), dioxin (TCDD), and fine particulate matter (PM2.5), across three time points in mice exposed two weeks prior to conception through gestation and lactation. After being exposed to toxicants during the embryonic and early postnatal developmental stages, 1,025 omics datasets were generated from the liver and analyzed across three mouse life stages. We discovered a significant sex-biased molecular response to distinct exposures in the liver at both the transcriptomic and epigenetic levels, showing dynamic changes across mouse development and aging. The perturbed pathways and transcription factors in response to different chemical exposures in both sexes were further evaluated to measure the sex-specific impact of each toxic exposure in the liver. Overall, this study presents the most detailed investigation of sex-specific molecular signatures under the influence of developmental exposures to toxic substances.

Contamination of agricultural soils with per and poly-fluoroalkyl substances (PFAS) is now widespread and common throughout the world due to management practices such as biosolid application. Crop and pasture plants can readily take up and accumulate PFAS in their tissues, which eventually ends up in food products or livestock feed and presents health issues. We investigated whether arbuscular mycorrhizal (AM) fungi in the soil affect plant PFAS uptake in three important cereal crop species (barley, bread wheat, durum wheat), using a combination of soils that were artificially-spiked or naturally contaminated with PFAS. Spiking soil with PFAS did not interfere with AM colonisation of roots, nor did it detrimentally affect plant biomass. However, the shoots of all three plant species accumulated high concentrations of multiple short- and long-chain PFAS compounds. Inoculation with AM fungi led to increased concentration of all measured PFAS compounds in durum wheat shoots and several compounds in barley shoots, with no effect on any compounds in bread wheat shoots. The effect of AM fungal colonisation on PFAS concentrations in cereal plants is highly dependent on the nature of the soil PFAS contamination (i.e., the concentration and speciation) and the host plant species. It remains to be investigated whether AM fungi can directly take up PFAS from the soil.